title: [Maternal-placental interactions and fetal programming].
abstract: Pregnancy-related complications not only represent a risk for maternal and fetal morbidity and mortality, but are also a risk for several diseases later in life. Many epidemiological studies have shown clear associations between an adverse intrauterine environment and an increased risk of diabetes, hypertension, cardiovascular disease, depression, obesity, and other chronic diseases in the adult. Some of these syndromes could be prevented by avoiding adverse stimuli or insults including psychological stress during pregnancy, intake of drugs, insufficient diet and substandard working conditions. Hence, all of these stimuli have the potential to alter health later in life. The placenta plays a key role in regulating the nutrient supply to the fetus and producing hormones that control the fetal as well as the maternal metabolism. Thus, any factor or stimulus that alters the function of the hormone producing placental trophoblast will provoke critical alterations of placental function and hence could induce programming of the fetus. The factors that change placental development may interfere with nutrient and oxygen supply to the fetus. This may be achieved by a direct disturbance of the placental barrier or more indirectly by, e. g., disturbing trophoblast invasion. For both path-ways, the respective pathologies are known: while preeclampsia is caused by alterations of the villous trophoblast, intra-uterine growth restriction is caused by insufficient invasion of the extravillous trophoblast. In both cases the effect can be undernutrition and/or fetal hypoxia, both of which adversely affect organ development, especially of brain and heart. However, the mechanisms responsible for disturbances of trophoblast differentiation and function remain elusive.
authors.affiliation: Institut für Anatomie und Zellbiologie, Universitätsklinikum RWTH Aachen, Deutschland.
authors.forename: M
authors.initials: M
authors.lastname: Kadyrov
authors.forename: G
authors.initials: G
authors.lastname: Moser
authors.forename: W
authors.initials: W
authors.lastname: Rath
authors.forename: N
authors.initials: N
authors.lastname: Kweider
authors.forename: C J
authors.initials: CJ
authors.lastname: Wruck
authors.forename: T
authors.initials: T
authors.lastname: Pufe
authors.forename: B
authors.initials: B
authors.lastname: Huppertz
mesh_terms: D000328:Adult; D005260:Female; D047109:Fetal Development; D005315:Fetal Diseases / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008431:Maternal-Fetal Exchange; D008954:Models, Biological; D010920:Placenta / Q000503:physiopathology*; D011247:Pregnancy